Abstract
In normal individuals hypoglycemic counterregulation is a multifactorial, redundant process that involves reduction of insulin secretion, increasing glucagon secretion, adrenergic activation, and increased growth hormone and cortisol secretion. Metabolically, these lead to increased glucose production, initially through glycogenolysis and later through gluconeogenesis, decreased muscle glucose oxidation and storage and increased release and use of alternative fuels, primarily free fatty acids. They also lead to hypoglycemic symptoms and hunger which increase food intake. These systems are designed to provide as much glucose as possible for brain glucose use. In patients with type 1 diabetes there are multiple impairments of these responses. Insulin does not decrease. Glucagon secretion is decreased or absent. Recovery from hypoglycemia is therefore dependent on the adrenergic response. Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both α and β adrenergic activity increase. Increased β-activity increases free fatty acid release which increase glucose production and decrease glucose utilization. The increased activitys primary role is to counteract β-adrenergic vasodilation. It may also reduce neurogenic and neuroglycopenic symptoms. Lastly, there is evidence that both cardiac and adrenergic sensitivity are altered in type 1 diabetes. It is hoped that this information can be used in the future to help develop ways to protect patients with type 1 diabetes from hypoglycemia and its adverse effects.
Keywords: muscle sympathetic nerve activity, epinephrine, type 1 diabetes, antecedent hypoglycemia, ACTH
Current Diabetes Reviews
Title: Sympathetic Mechanisms of Hypoglycemic Counterregulation
Volume: 3 Issue: 3
Author(s): Robert P. Hoffman
Affiliation:
Keywords: muscle sympathetic nerve activity, epinephrine, type 1 diabetes, antecedent hypoglycemia, ACTH
Abstract: In normal individuals hypoglycemic counterregulation is a multifactorial, redundant process that involves reduction of insulin secretion, increasing glucagon secretion, adrenergic activation, and increased growth hormone and cortisol secretion. Metabolically, these lead to increased glucose production, initially through glycogenolysis and later through gluconeogenesis, decreased muscle glucose oxidation and storage and increased release and use of alternative fuels, primarily free fatty acids. They also lead to hypoglycemic symptoms and hunger which increase food intake. These systems are designed to provide as much glucose as possible for brain glucose use. In patients with type 1 diabetes there are multiple impairments of these responses. Insulin does not decrease. Glucagon secretion is decreased or absent. Recovery from hypoglycemia is therefore dependent on the adrenergic response. Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both α and β adrenergic activity increase. Increased β-activity increases free fatty acid release which increase glucose production and decrease glucose utilization. The increased activitys primary role is to counteract β-adrenergic vasodilation. It may also reduce neurogenic and neuroglycopenic symptoms. Lastly, there is evidence that both cardiac and adrenergic sensitivity are altered in type 1 diabetes. It is hoped that this information can be used in the future to help develop ways to protect patients with type 1 diabetes from hypoglycemia and its adverse effects.
Export Options
About this article
Cite this article as:
Robert P. Hoffman , Sympathetic Mechanisms of Hypoglycemic Counterregulation, Current Diabetes Reviews 2007; 3 (3) . https://dx.doi.org/10.2174/157339907781368995
DOI https://dx.doi.org/10.2174/157339907781368995 |
Print ISSN 1573-3998 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6417 |
Call for Papers in Thematic Issues
Advancing Diabetic Wound Healing: Mechanisms and Interventions
In recent years, diabetic wounds have become a global health concern with the increase in the incidence of diabetes. Diabetic wounds are a kind of chronic and refractory ulcer. It is generally due to the microcirculatory disturbances and the reduced levels of endogenous growth factors. Delayed cutaneous wound healing is ...read more
Oxidative and inflammatory responses in the development of secondary diabetic complications
Diabetes, along with its associated secondary complications, represents a significant global health challenge, contributing significantly to morbidity and mortality. Unhealthy lifestyle habits, reduced physical activity, environmental pollutants, and stress are pivotal factors in the onset of diabetes, particularly type-2 diabetes. Poorly managed hyperglycemia can lead to various complications, including neuropathy, ...read more
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Properties and Potency of Small Molecule Agents for Treatment of Mycobacterium Tuberculosis Infections of the Central Nervous System
Central Nervous System Agents in Medicinal Chemistry Therapeutic Option of Plasmid-DNA Based Gene Transfer
Current Topics in Medicinal Chemistry Angiopoietin-1 and C16 Peptide Attenuate Vascular and Inflammatory Responses in Experimental Allergic Encephalomyelitis
CNS & Neurological Disorders - Drug Targets The Crosstalk between Tissue Engineering and Pharmaceutical Biotechnology: Recent Advances and Future Directions
Current Pharmaceutical Biotechnology Cellular and Molecular Regulation of Inflammatory Pain, Nociception and Hyperalgesia - The Role of the Transcription Factor NF-κB as the Lynchpin Nocisensor: Hyperalgesic or Analgesic Effect?
Current Immunology Reviews (Discontinued) Iron Oxide Nanoparticles: An Insight into their Biomedical Applications
Current Medicinal Chemistry Fibrosis and Regulation of Nerve Regeneration in the Peripheral and Central Nervous Systems
CNS & Neurological Disorders - Drug Targets GEMSP: A New Therapeutic Approach to Multiple Sclerosis
Central Nervous System Agents in Medicinal Chemistry PI3K/Akt Pathway: A Potential Therapeutic Target for Chronic Pain
Current Pharmaceutical Design Molecular Mechanisms, Biological Actions, and Neuropharmacology of the Growth-Associated Protein GAP-43
Current Neuropharmacology Current Clinical Applications of Botulinum Toxin
Current Pharmaceutical Design Caspases: Structure-Guided Design of Drugs to Control Cell Death
Mini-Reviews in Medicinal Chemistry Pharmacology of Ivabradine and the Effect on Chronic Heart Failure
Current Topics in Medicinal Chemistry A Review of Agents Patented for their Neuroprotective Properties
Recent Patents on CNS Drug Discovery (Discontinued) Role of Pituitary Adenylate Cyclase-Activating Polypeptide in Nociception and Migraine
CNS & Neurological Disorders - Drug Targets The Use of Stem Cells in Regenerative Medicine for Parkinson’s and Huntington’s Diseases
Current Medicinal Chemistry Ketamine: New Indications for an Old Drug
Current Drug Targets Fibromyalgia: The Prototypical Central Sensitivity Syndrome
Current Rheumatology Reviews Mesenchymal Stem Cell Research in Veterinary Medicine
Current Stem Cell Research & Therapy An Update on Drug Interactions with the Herbal Medicine Ginkgo biloba
Current Drug Metabolism